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SUMMARY The determinations of detailed stress states are of great importance for various environmental and engineering investigations, which makes numerical stress modelling a key issue in many fields. We developed a new stress modelling method governed by elastic wave equations using finite-difference scheme. By introducing an artificial damping factor to the particle velocity in wave modelling, the proposed method is able to solve both the dynamic stress evolution and the static stress state of equilibrium. We validate the proposed method both in body force and surface force benchmarks in different scales. With the proposed method, we are able to substantially improve the modelling accuracy of models in unbounded domain by using the perfectly matched layer as the artificial boundary conditions. A 3-D concrete-faced rockfill dam model is further presented as a numerical example of practical investigation. The consistent results with the finite-element method further illustrate the proposed method's applicability. As a minor modification to wave modelling scheme, the proposed stress modelling method is not only accurate for geological models through different scales, but also physically reasonable and easy to implement for geophysicists.

Hair follicle stem cells (HFSCs) are responsible for hair growth and hair follicle regeneration. MicroRNAs have been demonstrated to be involved in the differentiation of HFSCs. Thus, this study aimed to explore the potential role of miR-149 in the differentiation of HFSCs. The isolated HFSCs were identified by flow cytometric sorting. miR-149 expression was determined during differentiation of HFSCs. Gain- and loss-of-function approaches were conducted to explore the roles of miR-149, MAPK1/ERK2, and FGF2/c-MYC in colony formation and proliferation of HFSCs. Furthermore

Tunnel advance detection technology is an important method for determining the structure of a complex geological body in front of the tunnel face. Among the tunnel advance detection technologies, the seismic method is one of the most accurate methods with long detection distances. In seismic tunnel advance detection, the cylindrical configuration aggravates the complexity of the wave field in the tunnel space and significantly influences the accuracy of the detection results. Thus, it is crucial to simulate an accurate seismic full-wave field of the tunnel space and to understand the propagation and wave-field characteristics of individual seismic waves for seismic tunnel advance detection. Usually, in 3D Cartesian coordinates, the tunnel wall is approximated with a staircase boundary, but it is not sufficiently accurate in shape and generates numerical dispersion in the simulation, especially in the presence of surface waves. Therefore, we developed a variable staggered-grid finite-difference method in cylindrical coordinates to simulate the elastic full-wave field in a 3D tunnel space. Setting free-surface boundary conditions solves the propagation of surface waves on the tunnel wall and face. The free-surface boundary condition was validated by comparing the simulated seismic records with the finite element method. The interference of the instability and discontinuity of the pole axis in the seismic wave field simulation was eliminated using our method. Using this scheme, we simulated the elastic full-wave field of three geological bodies in front of the tunnel face, including the vertical interface, inclined interface, and karst cave. The results of the three models show that the excitation near the tunnel face is more conducive to the detection of geological bodies. Compared with the simulation results in Cartesian coordinates, the results in cylindrical coordinates show that numerical dispersion is negligible and conclude that a higher signal-to-noise ratio and more accurate seismic wave field can be simulated with cylindrical coordinates in the tunnel space. The new method can also be used as an accurate elastic wave propagator for reverse-time migration and full-waveform inversion under tunnel-observing geometries. Our simulation method provides theoretical and practical guidance for analyzing and interpreting seismic wave fields in tunnel advance detection.

Large roughness and structure disorder in ferroelectric ultrathin Langmuir-Blodgett (LB) film results in severe space scatter in electrical, ferroelectric and piezoelectric characteristics, thus limiting the nanoscale research and reliability of nano-devices. However, no effective method aiming at large-area uniform organic ferroelectric LB film has ever been reported to date. Herein, we present a facile hot-pressing strategy to prepare relatively large-area poly(vinylidene fluoride) (PVDF) LB film with ultra-smooth surface root mean square (RMS) roughness is 0.3 nm in a 30 μm × 30 μm area comparable to that of metal substrate, which maximized the potential of LB technique to control thickness distribution. More importantly, compared with traditionally annealed LB film, the hot-pressed LB film manifests significantly improved structure uniformity, less fluctuation in ferroelectric characteristics and higher dielectric and piezoelectric responses, owing to the uniform dipole orientation and higher crystalline quality. Besides, different surface charge relaxation behaviors are investigated and the underlying mechanisms are explained in the light of the interplay of surface charge and polarization charge in the case of nanoscale non-uniform switching. We believe that our work not only presents a novel strategy to endow PVDF LB film with unprecedented reliability and improved performance as a competitive candidate for future ferroelectric tunnel junctions (FTJs) and nano electro mechanical systems (NEMS), but also reveals an attracting coupling effect between the surface potential distribution and nanoscale non-uniform switching behavior, which is crucial for the understanding of local transport characterization modulated by band structure, bit signal stability for data-storage application and the related surface charge research, such as charge gradient microscopy (CGM) based on the collection of surface charge on the biased ferroelectric domains.

Some polymers are flexible, foldable, and wearable. Structural—functional composite is fabricated by adding inorganic fillers with functional properties. Up to date, compared with the polymer matrix, the composite prepared by polymer-inorganic fillers has lower flexibility, higher brittleness, and higher modulus of elasticity. In this paper, three-dimensional (3D) net-shaped submicron α-Al2O3, orthorhombic ZrO2, and rutile TiO2 fiber were fabricated by solution blowing spinning on a large scale. On the contrary, the elastic modulus (E) of the composite prepared by this 3D ceramic fiber was greatly reduced, and the flexibility of the composite was higher than that of the polymer matrix. When the strain was 75%, the E of the 3D net-shaped Al2O3 fiber-polydimethylsiloxane (PDMS) composite was 20% lower than that of PDMS. When the strain was 78%, the E of the 3D net-shaped TiO2 fiber-PDMS and 3D net-shaped ZrO2 fiber-PDMS composites decreased by 20% and 25%, respectively. This abnormal effect, namely the tunnel elastic enhancement effect, has great practical significance. In all-solid-state lithium-ion batteries, the composite inhibits lithium dendrite growth and the 3D inorganic network contributes to lithium ion transport. It is possible to promote the industrial production of low-cost and large-scale flexible solid-state lithium-ion batteries and it can enhance the energy storage density of energy storage materials. This novel idea also has bright prospects in flexible electronic materials.

Oxide-based ceramics could be promising thermoelectric materials because of their thermal and chemical stability at high temperature. However, their mediocre electrical conductivity or high thermal conductivity is still a challenge for the use in commercial devices. Here, we report significantly suppressed thermal conductivity in SrTiO3-based thermoelectric ceramics via high-entropy strategy for the first time, and optimized electrical conductivity by defect engineering. In high-entropy (Ca0.2Sr0.2Ba0.2Pb0.2La0.2)TiO3 bulks, the minimum thermal conductivity can be 1.17 W/(m·K) at 923 K, which should be ascribed to the large lattice distortion and the huge mass fluctuation effect. The power factor can reach about 295 μW/(m·K2) by inducing oxygen vacancies. Finally, the ZT value of 0.2 can be realized at 873 K in this bulk sample. This approach proposed a new concept of high entropy into thermoelectric oxides, which could be generalized for designing high-performance thermoelectric oxides with low thermal conductivity.

Hair follicles have been reported to contribute to epidermal healing, with differentiation of hair follicle stem cells (HFSCs) aiding in wound re-epithelialization. This study is aimed to delineate the molecular mechanistic actions by which prostate cancer-upregulated long noncoding RNA 1 (PlncRNA-1) accelerates the proliferation and differentiation of HFSCs in wound healing.HFSCs were obtained from the scalps of five volunteers, in which the expression of PlncRNA-1 and downstream regulatory genes was identified. Effects of PlncRNA-1 overexpression and ZEB1 knockdown on the proliferation and differentiation of HFSCs were examined. A wound mouse model was further established for in vivo experiments to substantiate in vitro findings.PlncRNA-1 is highly expressed in HFSCs and accelerates the proliferation and differentiation of HFSCs. PlncRNA-1 recruits EZH2 to ZEB1 promoter region and augments the H3K27me3 methylation, thereby downregulating the expression of ZEB1. Without such suppression, ZEB1 could repress MAPK1 expression and restrict HFSC proliferation and differentiation. Further, PlncRNA-1 overexpression accelerates wound healing and epidermal regeneration in vivo.PlncRNA-1 inhibits ZEB1 and activates MAPK1 signaling through upregulating EZH2, thereby enhancing the proliferation and differentiation of HFSCs and wound healing.

Fibroblast growth factor (FGF2) is reported to affect the proliferation, differentiation, and survival abilities of stem cells. In this study, we hypothesize that FGF2 might promote the differentiation of hair follicle stem cell (HFSCs) into endothelial cells (ECs), in a manner dependent on STAT5 activation. We first treated human HFSCs with recombinant human FGF2 to determine the involvement of FGF2 in the differentiation of HFSCs. Then the expression of EC-specific markers including von Willebrand factor (vWF), VE-cadherin, CD31, FLT-1, KDR and Tie2 was evaluated using immunofluorescence and flow cytometry, while the expression of HFSC-specific markers such as K15, K19, Lgr5, Sox9 and Lhx2 was determined by flow cytometry. Next, in vitro tube formation was performed to confirm the function of FGF2, and low-density lipoprotein (LDL) uptake by ECs and HFSCs was studied by Dil-acetylated LDL assay. In addition, we transduced FGF2-treated HFSCs with constitutive-active or dominant-negative STAT5A adenovirus vectors. FGF2 up-regulated the expression of EC-specific markers, and promoted the differentiation of HFSCs into ECs, tube formation and LDL uptake. The phosphorylated STAT5 was translocated into the nucleus of HFSCs after FGF2 treatment, but this translocation was blocked by the dominant-negative STAT5A mutant. FGF2 increased the differentiation potential through the activation of STAT5 in vivo. Taken together, we find that FGF2 promotes the differentiation of HFSCs into ECs via activated STAT5, which gives a new perspective on the role of FGF2 in the development of ischemic vascular disease.

Background Dysfunction of the DNA methylation was associated with stem cell reprogramming. Moreover, DNA methyltransferase 1 (DNMT1) deficiency was involved in the differentiation of hair follicle stem cell (HFSc), but the molecular mechanisms remain unknown. Methods HFSc from human scalp tissues were isolated and cultured. The oil red O staining was used to observe the adipogenesis. The interaction relationship between microRNA (miR)-214-3p and mitogen-activated protein kinase 1 (MAPK1) was accessed by dual-luciferase reporter gene assay. The methylation level of miR-214-3p promoter was detected by methylation-specific PCR and the enrichment of DNMT1 in miR-214-3p promoter by chromatin immunoprecipitation assay. A mouse model of trauma was established to observe the skin regeneration at 0, 6, and 14 days. Results Expression of DNMT1 and MAPK1 was increased in the HFSc, while the expression of miR-214-3p was reduced. Moreover, DNMT1 inhibited the expression of miR-214-3p by promoting the promoter methylation of miR-214-3p. Overexpression of DNMT1 could reduce the expression of miR-214-3p, but increase the expression of MAPK1 and the extent of extracellular signal regulated kinase (ERK)1/2 phosphorylation, leading to enhanced adipogenic differentiation. Importantly, DNMT1 promoted skin regeneration in vivo. Conversely, overexpression of miR-214-3p could reverse the effects of DNMT1 on adipogenesis of HFSc. Conclusion DNMT1 promotes adipogenesis of HFSc by mediating miR-214-3p/MAPK1/p-ERK1/2 axis. This study may provide novel biomarkers for the potential application in stem cell therapy.

Background Dysfunction of the DNA methylation was associated with stem cell reprogramming. Moreover, DNA methyltransferase 1 (DNMT1) deficiency was involved in the differentiation of hair follicle stem cell (HFSc), but the molecular mechanisms remain unknown. Methods HFSc from human scalp tissues were isolated and cultured. The oil red O staining was used to detect the adipogenesis. The interaction relationship between microRNA (miR)-214-3p and mitogen-activated protein kinase 1 (MAPK1) was accessed by dual-luciferase reporter gene assay. The methylation level of miR-214-3p promoter was detected by methylation-specific PCR, and the enrichment of DNMT1 in miR-214-3p promoter was detected by chromatin immunoprecipitation assay (ChIP). The mouse model of trauma was established to observe the skin regeneration at 0, 6 and 14 days. Results Expression of DNMT1 and MAPK1 was increased in the HFSc, while the expression of miR-214-3p was reduced. Moreover, DNMT1 inhibited the expression of miR-214-3p by promoting the promoter methylation of miR-214-3p. Overexpression of DNMT1 could reduce the expression of miR-214-3p but increased the expression of MAPK1 and the extent of extracellular signal regulated kinase (ERK)1/2 phosphorylation. DNMT1 also significantly enhanced the adipogenic differentiation, and increased the proportion and markers of adipogenic cells. Importantly, DNMT1 promoted skin regeneration in vivo. Conversely, overexpression of miR-214-3p could reverse the effects of DNMT1 on adipogenesis of HFSc. Conclusion DNMT1 promotes adipogenesis of HFSc by mediating miR-214-3p/MAPK1/phosphorylated-ERK1/2 axis. This study may provide more biomarkers for the potential application in stem cell therapy.

Because of the high carrier concentration, copper telluride (Cu2Te) has a relatively low Seebeck coefficient and high thermal conductivity, which are not good for its thermoelectric performance. To simultaneously optimize carrier concentration, lower thermal conductivity and improve the stability, BiCuTeO, an oxygen containing compound with lower carrier concentration, is in situ formed in Cu2Te by a method of combining self-propagating high-temperature synthesis (SHS) with spark plasma sintering (SPS). With the incorporation of BiCuTeO, the carrier concentration decreased from 8.1 × 1020 to 3.8 × 1020 cm−3, bringing the increase of power factor from ~1.91 to ~2.97 μW cm−1 K−2 at normal temperature. At the same time, thermal conductivity reduced from 2.61 to 1.48 W m−1 K−1 at 623 K. Consequently, (Cu2Te)0.95-(BiCuTeO)0.05 composite sample reached a relatively high ZT value of 0.13 at 723 K, which is 41% higher than that of Cu2Te.

BRAF-activated non-coding RNA (BANCR) is a long non-coding RNA (lncRNA) that contributes to the initiation and development of many solid tumors, including melanoma. However, the BANCR functions and downstream mechanisms are largely unknown. In this study, we aim to investigate how BANCR participates in the proliferation and migration of malignant melanoma and elucidate the underlying mechanism in this process. We found that the expression of the BANCR was low in melanocytic nevus and human melanocytes but high in melanoma tissues and cell lines. Knockdown of BANCR inhibited melanoma cell proliferation and invasion, and induced cell apoptosis. The decreased expression of relative marker proteins further demonstrated the inhibitory effect of BANCR siRNA in cell growth and migration. Then, we detected downregulation of microRNA-204 (miR‑204), a suppressor of melanoma growth, in melanoma tissues and cell lines. We identified that miR‑204 was a direct target of BANCR and neurogenic locus notch homolog protein 2 (Notch2) was a direct target of miR‑204. BANCR may promote melanoma cell growth through inhibition of miR‑204, leading to the activation of Notch2 pathway. By tumorigenicity assay in BALB/c nude mice, we further demonstrated that BANCR knockdown inhibited tumor growth in vivo. Our results suggest the BANCR/miR‑204/Notch2 axis mediates melanoma cell proliferation and tumor progression.

Aims The purpose of this study was to explore the precise role and mechanism of p38 inhibiting cutaneous squamous cell carcinoma associated lincRNA (PICSAR) in CSCC. Materials and methods The expression levels of PICSAR, microRNA-125b (miR-125b) and yes-associated protein1 (YAP1) were determined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation, apoptosis and invasion were evaluated by Cell Counting Kit-8 (CCK-8) assay, flow cytometry, transwell assay, respectively. The interaction between miR-125b and PICSAR or YAP1 was predicted by bioinformatics software and confirmed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Western blot was employed to detect the protein expression of YAP1. The mice xenograft model was established to investigate the role of PICSAR in vivo. Key findings PICSAR was upregulated in CSCC tissues and cells. PICSAR knockdown inhibited cell proliferation and invasion and induced apoptosis in CSCC cells. Moreover, miR-125b could directly bind to PICSAR and its inhibition reversed the effect of PICSAR knockdown on proliferation, invasion and apoptosis in CSCC cells. In addition, YAP1 was a direct target of miR-125b and its overexpression attenuated the anti-cancer role of miR-125b in CSCC cells. Furthermore, YAP1 expression was positively regulated by PICSAR and negatively regulated by miR-125b. Besides, interference of PICSAR suppressed tumor growth by upregulating miR-125b and downregulating YAP1. Significance PICSAR knockdown suppressed cell proliferation and invasion and promoted apoptosis in CSCC cells by regulating miR-125b/YAP1 axis, providing new sights for treatment of CSCC.

Condyloma acuminata are a type of verrucous hyperplasia in the genital and perianal areas caused by human papilloma virus (HPV) infection. Traditional treatment methods for condyloma acuminata, such as topical medications, carbon dioxide (CO2) laser, cryotherapy, and surgical excision, can be effective at removing warts, however, they do not eliminate subclinical and latent HPV infection, resulting in a high recurrence rate and even leaving trauma and scars. We report a case of condyloma acuminata covering the glans penis, considering our patient had a singular, large lesion, thus, to reduce the risk of recurrence and minimize the trauma caused by treatment, we chose ALA/photodynamic therapy (ALA-PDT). We provided eight rounds of ALA-PDT at a treatment interval of 7 days, the skin lesion disappeared completely, leaving a chapped, flushed glans without scarring. There was no recurrence during the 6-month follow-up period. Thus, we firmly believe that ALA-PDT is an effective, safe, and curative treatment, and is worth popularizing in clinical practice.

Ultrahigh energy density dielectric film Dielectrics help hold charge as capacitors and are fundamental energy storage components. Improving energy density and other properties may help these materials be more competitive with batteries for energy storage applications. Pan et al. introduced a specific type of nanodomain structure in a BiFeO 3 -BaTiO 3 -SrTiO 3 solid solution that dramatically increased the energy density. The nanodomains were organized so as to minimize energy loss during polarization switching. The enhancement in the dielectric properties suggests that the strategy may be useful for designing high-performance dielectrics. Science , this issue p. 578

Long non-coding RNAs (lncRNAs) are defined as non-coding transcripts (>200 nucleotides) that serve important roles in the proliferation and differentiation of stem cells. Hair follicle stem cells (HFTs) have multidirectional differentiation potential and are able to differentiate into skin, hair follicles and sebaceous glands, serving a role in skin wound healing. The aim of the present study was to analyze the regulatory role of lncRNA AK015322 (IncRNA5322) in HFTs and the potential mechanism of IncRNA5322‑mediated differentiation of HFTs. The results demonstrated that lncRNA5322 transfection promoted proliferation and differentiation in HFTs. It was identified that lncRNA5322 transfection upregulated the expression and phosphorylation of phosphoinositide 3‑kinase (PI3K) and protein kinase B (AKT) in HFTs. It was also observed that lncRNA5322 transfection upregulated microRNA (miR)‑21 and miR‑21 agonist (agomir‑21) eliminated lncRNA5322‑induced expression and phosphorylation of PI3K and AKT. The present study also demonstrated that agomir‑21 blocked IncRNA5322‑induced expression and phosphorylation of PI3K and AKT in HFTs. The results indicated that agomir‑21 transfection also suppressed the IncRNA5322‑induced proliferation and differentiation of HFTs. In conclusion, the results of the present study suggest that lncRNA5322 is able to promote the proliferation and differentiation of HFTs by targeting the miR‑21‑mediated PI3K‑AKT signaling pathway in HFTs.

The proliferation and differentiation of hair follicle stem cells (HFSCs) is regulated by several signaling pathways, including BMP and PTEN. Therefore, this study intended to clarify the potential effects of two such regulators, BMP2 and PTEN, on HFSC differentiation. HFSCs were subjected to BMP2, noggin (BMP2 ligand inhibitor), rapamycin (Rapa, autophagy inducer), 3-methyladenine (3-MA, autophagy inhibitor), or shRNA against PTEN. The differentiation of HFSCs was evaluated using oil red O staining and autophagy was assessed using the transmission electron microscope. Then expression of epidermal differentiation marker (K10 and involucrin), adipogenic markers (PPAR-γ2, aP2, perilipin2, and Adipoq), keratinocyte-specific marker (K15), proliferation-related markers (PCNA and Ki67) and autophagy-related factors (Atg5, Atg7, Atg12, Beclin-1 and LC3-II/LC3-I) was examined by RT-qPCR and Western blot analysis. Next, HFSCs were treated with 3-MA, or shRNA against Atg5 or Atg7 to verify the effect of autophagy on differentiation of BMP2-treated HFSCs. Finally, the effect of BMP2 on HFSC differentiation was verified by a mouse wound model. HFSCs overexpressing BMP2 exhibited elevated expression of epidermal differentiation marker, adipogenic markers and autophagy-related factors but inhibited expression of keratinocyte-specific marker and proliferation-related markers. Furthermore, we found that PTEN promoted the differentiation of BMP2-treated HFSCs by inducing autophagy. In vivo experiments further confirmed the roles of BMP2/PTEN on differentiation of HFSCs. Taken together, BMP2 up-regulated PTEN and consequently induced autophagy to facilitate HFSC differentiation.

MicroRNAs (miRNAs) have been widely accepted to play important roles in the regulation of keratinocyte functions. Here, we aimed to further explore the role and underlying mechanism of miR-125b-5p and miR-181b-5p in psoriasis. The expression levels of miR-125b-5p, miR-181b-5p and Akt3 mRNA were detected by qRT-PCR assay. Cell proliferation ability was determined by MTT assay and BrdU incorporation assay. Dual-luciferase reporter assay and RNA Immunoprecipitation assay were used to confirm the targeted interaction between miR-125b-5p or miR-181b-5p and Akt3 in human epidermal keratinocytes (HEKs). The levels of ki-67, Akt3 protein, Akt, p-Akt, mTOR and p-mTOR were measured by Western blot. Our study indicated that miR-125b-5p and miR-181b-5p were downregulated (about 61.3% with miR-125b-5p and 60.4% with miR-181b-5p) and Akt3 was upregulated (about 2.68-fold) in psoriasis. Upregulation of miR-125b-5p or miR-181b-5p resulted in about a 33% or 40% reduction of HEKs proliferation in vitro, while Akt3 overexpression triggered a 1.3-fold enhancement on HEKs proliferation. Akt3 was a direct target of miR-125b-5p or miR-181b-5p. Moreover, HEKs proliferation ability in cotransfection of miR-125b-5p mimics (or miR-181-5p mimics) and vector-Akt3 group was about 2-fold (or 1.98-fold) that in the miR-125b-5p mimics (or miR-181-5p mimics) alone group. Akt/mTOR signaling was involved in miR-125b-5p mimics- or miR-181b-5p mimics-mediated inhibition effect on HEKs proliferation. Our study suggested that the upregulation of miR-125b-5p or miR-181b-5p inhibited HEKs proliferation at least partly by targeting Akt3, providing novel mechanisms of miRNAs involved in psoriasis.